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Potential of Fenugreek in Management of Fibrotic Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Amit D. Kandhare, Sunil Bhaskaran, Subhash L. Bodhankar
Subsequently, the potential of glycosides-based standardized fenugreek seed extract (SFSE-G) against experimental pulmonary fibrosis induced by bleomycin was reported (Kandhare et al. 2015). In this study, SFSE-G (5, 10, 20, and 40 mg/kg) orally administered in fibrotic rats for 28 days ameliorated bleomycin-induced pulmonary fibrosis biphasic response. In the initial phase (16 days), the elevated inflammatory response was significantly reduced by SFSE-G via inhibition of the release of various mediators, including 5-hydroxytryptamine, TNF-α, ILs in the lungs, and bronchoalveolar lavage fluid (BALF). The attenuation of elevated oxido-nitrosative stress (superoxide dismutase (SOD), glutathione (GSH), MDA, myeloperoxidase (MPO), nitric oxide (NO), nuclear factor E2-related factor (Nrf2), and Heme oxygenase 1 (HO-1)) was observed. Furthermore, SFSE-G treatment inhibited the second phase of fibrogenic changes (day 16–28) via fibrotic and apoptotic mediators such as collagen-1, endothelin-1 (ET-1), mucin 5ac (Muc5ac), mothers against decapentaplegic homolog-3 (Smad3), nuclear factor-kappa B (NF-kB), TGF-β, VEGF, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated x protein (Bax), and Caspase-3. The histological findings from lung tissue corroborated with the biochemical results and indicated the anti-fibrotic efficacy of SFSE-G against bleomycin-induced pulmonary fibrosis. The author concluded that glycosides-based standardized fenugreek seed extract ameliorated pulmonary fibrosis via activation of the Nrf2 pathway and inhibition of TGF-β (Kandhare et al. 2015).
Cytotoxic Phenanthridone Alkaloid Constituents of the Amaryllidaceae
Published in Spyridon E. Kintzios, Maria G. Barberaki, Evangelia A. Flampouri, Plants That Fight Cancer, 2019
Jerald J. Nair, Johannes van Staden
General and specific terms: AIF, apoptosis inducing factor; AKT, protein kinase B; ATM, ataxia telangiectasia mutated; ATR, ataxia telangiectasia and Rad3-related protein; Bax, Bcl-2 associated X-protein; Bcl-2, B-cell lymphoma 2; Bid, BH3-interacting domain death agonist; c-Abl, Abelson murine leukemia viral oncogene homolog 1; DNA-PK, DNA-dependent protein kinase; DR, death receptor; EC, endothelial cell; eEF1A, eukaryotic translation elongation factor 1 alpha; HUVEC, human umbilical vein endothelial cell; JNK, c-Jung N-terminal kinase; LPS, lipopolysaccharide; Mcl-1, induced myeloid leukemia cell differentiation protein; MMP, mitochondrial membrane permeabilization; MND, motor neuron disease; NF-κB, nuclear factor κB; NHF, normal human fibroblast; NO, nitric oxide; NOAEL, no adverse effect level; p53, tumor suppressor protein; PARP, poly(ADP-ribose) polymerase; PBMC, peripheral blood mononuclear cell; PCD, programmed cell death; PI(3)kinase, phosphoinositide 3 kinase; ROS, reactive oxygen species; SAPK, stress-activated protein kinase; TAM, Tamoxifen; T/C, treatment to control index; TNF, tumor necrosis factor; TM, traditional medicine; VEGF, vascular endothelial growth factor.
Mitochondrial Dysfunction in Chronic Kidney Disease
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Maria V. Irazabal, Alfonso Eirin
Tubular cell apoptosis is an important pathological feature of PKD and has been reported both in experimental models and humans (Ali et al. 2000). B-cell lymphoma-2 deficiency in mice is associated with increased apoptosis and severe PKD-like changes in the proximal and distal tubular segments (Nakayama et al. 1994; Veis et al. 1993). Contrarily, renal expression of Bcl-2-associated X protein remains unchanged in PKD rat kidneys (Ecder et al. 2002), suggesting that an imbalance between pro- and anti-apoptotic factors may contribute to programed cell death in experimental PKD.
Pyroptosis in neurodegenerative diseases: What lies beneath the tip of the iceberg?
Published in International Reviews of Immunology, 2023
Mengli Yue, Li Xiao, Rui Yan, Xinyi Li, Wei Yang
In the Mitochondrial-dependent intrinsic apoptotic pathway, mitochondrial outer membrane permeabilization (MOMP) by Bak/Bax is triggered by apoptotic stimuli such as cytotoxic drugs, DNA damage, iron induced oxidative stress. The dynamic balance between pro- and anti-apoptotic members of the B cell lymphoma 2 (BCL-2) protein family is responsible for mitochondrial outer membrane integrity. It has been confirmed that the pro-apoptotic BCL-2 proteins BCL-2-associated X protein (BAX) and BCL-2 antagonist, or killer (BAK) are required for MOMP, but the specific mechanism between MOMP and Bak/Bax is not very clear [31]. When MOMP occurs, mitochondrial proteins, such as cytochrome c, can enter the cytoplasm to initiate the assembly of inflammasome and promote the autocleavage of caspase-9. Caspase-9 acts on downstream caspase 3 and mediates pyroptosis through caspase-3 cleavage of a GSDME [32,33].
Apoptosis targeted therapies in acute myeloid leukemia: an update
Published in Expert Review of Hematology, 2020
Somedeb Ball, Gautam Borthakur
Cellular apoptosis is orchestrated through two distinct but interconnected pathways. The intrinsic pathway involves mitochondria in leading to the formation of apoptosome. Activation of this pathway in response to apoptotic stimuli is mainly controlled by the BCL2 family of proteins. These include several pro-apoptotic BCL2- homology 3 (BH3)- only proteins (e.g. BH3-interacting domain death agonist (BID), BCL2 antagonist of cell death (BAD), BCL2- interacting killer (BIK), BCL2- like protein 11 (BIM), p53-upregulated modulators of apoptosis (PUMA), phorbol-12-myristate-13-acetate-induced protein 1(NOXA), etc.), members with anti-apoptotic activity (e.g. BCL2, BCL-XL, myeloid cell leukemia-1 (MCL1), etc.), and some pro-apoptotic effector proteins (e.g. BCL2-associated X protein (BAX), BCL2-antagonist/killer (BAK), etc.) [9]. Apoptotic stimuli lead to the upregulation of pro-apoptotic molecules and downregulation of anti-apoptotic ones, resulting in an imbalance between pro- and anti-apoptotic proteins in the cellular environment, which in turn activates the effector proteins, BAX and BAK. The dimerization of BAX and BAK in the mitochondrial membrane increases its permeability, releasing cytochrome C into the cytosol. It then forms an apoptosome with the incorporation of apoptotic protease activating factor 1 (APAF-1) and procaspase 9, which on activation gets converted to caspase-9 to mediate the proteolysis and further activation of other caspases [10].
Characterization of in vitro and in vivo metabolism of leelamine using liquid chromatography-tandem mass spectrometry
Published in Xenobiotica, 2019
Riya Shrestha, Jung Jae Jo, DooHyun Lee, Taeho Lee, Sangkyu Lee
Leelamine (Figure 1), a dehydroabietylamine derivative of dehydroabietic acid, is found in the resins of pine trees (Kovaleva et al., 2017). It is a pyruvate dehydrogenase kinase 4 (PDK4) inhibitor and has been found to exhibit hypoglycemic activity in ob/ob mice and inhibit glyceroneogenesis in isolated adipocytes by activating the pyruvate dehydrogenase complex (PDC) (Cadoudal et al., 2008; Jeoung & Harris, 2010). Leelamine as a drug has been of considerable interest recently because it has been effective in the treatment of melanoma by disrupting cholesterol homeostasis in cancer cells (Gowda et al., 2017; Kuzu et al., 2014). It exhibits a strong anticancer effect on human breast cancer cell lines by generating reactive oxygen species and inducing B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax)/Bcl-2 homologous antagonist/killer (Bak)-dependent apoptosis (Sehrawat et al., 2017). Moreover, our previous study in mice showed that leelamine is a potent and selective inducer of CYP2B activity, but has a low oral bioavailability of 7.6% (Sim et al., 2015; Song et al., 2013).